IL5 induces B cell proliferation and immunoglobulin (Ig) secretion and results in appearance of a phenotypically novel B cell population which expresses high density of CD44 and low densities of B220 (CD45) and Ia.This B cell subpopulation mediates nearly all of the proliferative and Ig secretory activity of IL5-activated B cells. In addition, the CD44 expressed by these cells mediates binding to the extracellular matrix material hyaluronic acid (HA), indicating a potential role for CD44 in regulating trafficking of activated B cells in vivo. The CD44 expressed on IL5-stimulated B cells migrates with a lower molecular weight than does CD44 expressed by control B cells, reflecting differential glycosylation. Other B cell activating stimuli such as LPS do not induce CD44-dependent HA-binding activity. However, LPS-activated B cells demonstrate CD44-dependent HA binding rapidly after exposure to a unique CD44-specific mAb, suggesting that distinct functional states of the CD44 molecule exist, perhaps reflecting differences in conformation or cytoskeletal association. A series of mAb was generated by immunizing rats with activated mouse B cells. One of these mAb (GL7) reacts with a subpopulation of activated B cells, as well as with activated T cells. GL7 precipitates what appears to be a previously undescribed 29-31 KDa molecule from activated B cells. Another mAb generated in this fashion (GL1) reacts with activated B but not T cells. GL1 inhibits responses of CD4+ T cells to activated B cells, suggesting that the target of GL1 may represent a costimulatory molecule for T cell activation. To establish a system for the study of Th cell-B cell interaction at a single cell level, responses were generated using Ig transgenic B cells and cloned Th cells. Highly efficient hapten-specific responses were generated. The study of sera from these transgenic mice indicated that transgene-associated idiotype was expressed in association with endogenous Ig molecules. This association was shown to result from the formation of hybrid Ig molecules in which transgenic mu chains are associated with endogenous mu or alpha heavy chains.